BACKGROUND:Traumatic brain injury (TBI) triggers a cascade of secondary damage, including neuroinflammation, astrocyte activation, and disruption of the blood-brain barrier (BBB), all of which contribute to long-term neurological deficits. Astrocyte-derived exosomes have emerged as a promising therapeutic avenue; however, the specific contributions of their molecular cargo remain poorly understood. This study explores whether astrocyte-derived exosomal delivery of microRNA-211-5p (miR-211-5p) can attenuate secondary injury and enhance functional recovery following TBI. METHODS:Primary astrocytes were transfected with AAV-rno-miR-211-5p, and the resulting exosomes were isolated and characterized. TBI was induced in adult rats using a controlled cortical impact (CCI) model. Exosomes (1 × 1011 particles) were administered intravenously 30 min post-injury. Behavioral assessments were conducted to evaluate cognitive function and neurological deficits. Brain edema, glial activation, and the expression of inflammatory cytokines (IL-6, IL-1β, TNF-α) and BBB-related markers-including glial fibrillary acidic protein (GFAP), matrix metalloproteinase 9 (MMP9), aquaporin 4 (AQP4), and the tight junction proteins zonula occludens-1 (ZO-1) and claudin-5-were analyzed using quantitative real-time PCR, Western blotting, enzyme-linked immunosorbent assay, and histopathological techniques. RESULTS:Exosomes enriched with miR-211-5p significantly improved cognitive and neurological outcomes, reduced cerebral edema, and downregulated the expression of GFAP, MMP9, and AQP4. Furthermore, the integrity of the BBB was preserved, as evidenced by sustained expression of ZO-1 and claudin-5. Levels of the proinflammatory cytokines IL-6, IL-1β, and TNF-α were also markedly decreased in the injured cortex. CONCLUSION:Astrocyte-derived exosomal miR-211-5p confers neuroprotection in TBI by modulating glial activation, reducing neuroinflammation, and preserving BBB integrity. These findings underscore the therapeutic potential of miR-211-5p-loaded exosomes as a cell-free, targeted intervention for brain trauma.

Lipid droplet (LD) accumulation in microglia results in a dysfunctional and proinflammatory state after ischemic stroke and worsens neurological outcomes; yet how this accumulation is regulated remains unclear. Interferon regulatory factor 7 (IRF7) is an immune regulatory factor whose role in lipid metabolism and autophagy has been increasingly studied in peripheral tissues. However, the role of IRF7 in microglial lipophagy (a selective autophagic process that targets LDs) and poststroke functional recovery remains unexplored. In this study, using a mouse photothrombotic ischemia (PTI) model, we observed that microglia in the peri-infarct region displayed persistent lipophagy impairment and LD accumulation for up to 21 days. Reanalysis of the single-cell RNA sequencing (scRNA-seq) dataset revealed that an Irf7high microglial MG1 subcluster (disease-associated microglia) was significantly associated with autophagy and lipid metabolism poststroke. Furthermore, microglial Irf7 conditional knockout (Irf7 cKO) mice exhibited a significant rescue of lipophagy impairment and an alleviation of the ensuing LD accumulation in microglia, accompanied by enhanced synaptic plasticity and motor functional recovery during the subacute phase poststroke. Consistently, in the 15-month-old distal middle cerebral artery occlusion (dMCAO) model, Irf7 cKO mice also displayed similar improvements. Similar results were also observed in vitro. Mechanistically, Gnai2 was identified as a positively regulated transcriptional target of IRF7. In BV2 cells and primary microglia, Gnai2 knockdown mitigated lipopolysaccharide (LPS)-induced lipophagy impairment, thereby reducing LD accumulation. This treatment also increased the level of phosphatidylcholine (PC), a key lipid for stabilizing small LDs as well as promoting autophagosome formation and autophagic flux. Consistently, microglial Irf7 deletion or knockdown attenuated stroke- or LPS-induced PC reduction both in vivo and in vitro. Furthermore, exogenous supplementation with CDP-choline, an intermediate in PC synthesis, alleviated LD accumulation and lipophagy impairment, thereby improving motor function. Additionally, delayed administration of an inhibitor of stimulator of interferon genes (STING, an upstream target of IRF7) replicated the beneficial effects observed in Irf7 cKO mice, and its effects were not further enhanced by microglial Irf7 deletion. Taken together, these novel findings reveal that persistent impairment of microglial lipophagy is a key contributor to poststroke LD accumulation, and that IRF7 is involved in this process through direct transcriptional activation of Gnai2, which reduces the PC levels. Suppressing IRF7 with a STING inhibitor is a potential strategy for modulating microglial lipid metabolism and promoting functional recovery following stroke.

BackgroundIntracerebral hemorrhage (ICH) is a severe neurological condition with high morbidity and mortality rates. Robot-Assisted Minimally Invasive Surgery (RA-MIS) has emerged as a novel technique that may offer advantages over traditional craniotomy. This study aims to evaluate the clinical efficacy of RA-MIS compared to conventional craniotomy in patients with ICH.MethodsA retrospective cohort study was conducted involving 44 patients with ICH admitted to two medical centers between December 1, 2022, and October 31, 2024. Patients were divided into two groups: 24 underwent RA-MIS, and 20 underwent traditional craniotomy. Baseline characteristics, functional outcomes [modified Rankin Scale (mRS)], neurological deficits [National Institutes of Health Stroke Scale (NIHSS)], postoperative complications, hospitalization costs, duration of respiratory support, and mortality rates were analyzed.ResultsThe RA-MIS group demonstrated significantly better functional outcomes at 90 days postoperative, with a mean mRS score of 2.58 ± 1.72 compared to 3.85 ± 1.63 in the craniotomy group (P = 0.017). NIHSS scores at 90 days were also significantly lower in the RA-MIS group (3.64 ± 3.32 vs. 7.71 ± 5.35; P = 0.006), indicating improved neurological recovery. RA-MIS patients experienced fewer postoperative complications, including lower incidences of pneumonia (16.7% vs. 70.0%; P < 0.001) and intracranial infections (0.0% vs. 20.0%; P = 0.036). The total hospitalization costs were significantly lower for the RA-MIS group (¥78,677 ± 38,904 vs. ¥136,399 ± 85,916; P = 0.006), and the duration of respiratory support was shorter (64.00 ± 161.79 h vs. 238.25 ± 197.04 h; P = 0.002). The mortality rate was significantly lower in the RA-MIS group (8.3% vs. 30.0%; P = 0.020).ConclusionsRA-MIS is associated with improved functional and neurological outcomes, fewer postoperative complications, reduced hospitalization costs, and lower mortality rates compared to traditional craniotomy in patients with ICH. These findings suggest that RA-MIS may be a more effective and economical surgical option for hematoma evacuation in ICH patients.

Background: IgG4-related hypertrophic pachymeningitis (IgG4-RHP) is an extremely rare central nervous system (CNS) autoimmune disorder, characterized by dural thickening, space-occupying effects, and neurological compression symptoms. It is frequently misdiagnosed as meningioma due to overlapping radiological features, leading to inappropriate management. This study aims to report a unique case of IgG4-RHP with skull destruction and subcutaneous mass formation, and summarize its diagnostic and therapeutic strategies through literature review. Methods: A 53-year-old male with a chronic subdural hematoma history was admitted for a progressive right frontal subcutaneous mass. Preoperative computed tomography (CT) and magnetic resonance imaging (MRI) were performed, followed by staged surgeries (subcutaneous biopsy and craniotomy with subtotal resection). Histopathological examinations (Hematoxylin and Eosin staining, IgG/IgG4 immunostaining) and serum IgG4 detection were conducted. The patient received postoperative prednisone acetate (60 mg/d) and 3-month follow-up. A literature search was also performed to analyze 34 previously reported IgG4-RHP cases. Results: Histopathology showed dense lymphoplasmacytic infiltration, storiform fibrosis, ≈40 IgG4+ plasma cells per high-power field (HPF), and an IgG4+/IgG+ ratio of ≈30%. Serum IgG4 was significantly elevated to 1521 μg/mL (normal < 1350 μg/mL), with marked reduction in residual lesions on follow-up MRI. Literature review revealed a 73.5% male predominance, mean age of 48.6 years, headache as the most common symptom (58.8%), and a 38.5% misdiagnosis rate. Glucocorticoids alone or combined with immunosuppressants achieved favorable outcomes in 96.0% of treated cases. Conclusions: Histopathological examination combined with serum IgG4 detection is the gold standard for IgG4-RHP diagnosis. Surgical resection relieves mass-occupying effects, while glucocorticoids are first-line therapy. Long-term follow-up is necessary for recurrence monitoring, and rituximab is effective for refractory cases. Awareness of atypical manifestations like skull destruction can reduce misdiagnosis and improve outcomes.

This study systematically compares various methods for calculating brainstem hematoma volume, and introduces a novel estimation method based on the maximum cross-sectional area. First, we assessed the accuracy of the Tada formula and 3D Slicer software for quantifying brainstem hematomas of different sizes and morphologies. The results revealed significant differences among methods, with the traditional Tada formula frequently overestimating hematoma volumes. We therefore propose an improved algorithm that substantially increases both the accuracy and reliability of hematoma volume assessment. Experimental results demonstrate that this new method provides greater precision and consistency when measuring the volume of irregular hematomas. These findings not only contribute to improved diagnosis and treatment of brainstem hemorrhage but also provide valuable support for future research and practical applications.

BackgroundThe optimal timing of cranioplasty (CP) after decompressive craniectomy (DC) is inconclusive. This article aims to investigate the effect of different timing of CP on the neurologic prognosis of patients, and to explore the feasibility and safety of ultra-early CP (within 3 weeks) following DC.MethodsThe duration time of surgery, intraoperative bleeding volume, surgery-related complications, and activities of daily living (ADL) scores were retrospectively analyzed in 23 patients underwent ultra-early CP performed within 3 weeks, and compared with 136 patients with non-ultra-early CP performed within the same time period.ResultsThe mean duration time of surgery in the ultra-early group was significantly shorter than that in the non-ultra-early group. ADL scores were significantly lower in the ultra-early group than in the non-ultra-early group both before and 1 month after CP, but there was no statistically significant difference in ADL scores between the two groups at long-term follow-up. The overall incidence of surgery-related complications was 17.39% (4/23) in the ultra-early group and 14.71% (20/136) in the non-ultra-early group, and there was no statistically significant difference in the comparison between the two groups (p = 0.739).ConclusionBoth ultra-early and non-ultra-early CP can significantly improve the neurological prognosis of patients. Ultra-early CP can significantly shorten the length of surgery and does not increase the incidence of surgery-related complications, which has a certain degree of safety and feasibility, and can be popularized under the premise of strict screening of indications, but further research is still needed.

Glioblastoma (GBM), as one of the most common and aggressive primary brain tumors, pose significant challenges in diagnosis and treatment, highlighting the urgent need for the identification of novel biomarkers, NFKBIE, which may play a critical role in tumor progression, immune modulation, and therapeutic response. We investigated the role of NFKBIE in GBM through both bioinformatics analysis and experimental validation. Initially, bioinformatics analysis based on public databases revealed significant differential expression of NFKBIE across various cancer types, particularly in GBM, where elevated expression was correlated with poor patient prognosis, including overall survival, disease-specific survival, and progression-free survival. Furthermore, genetic alterations in NFKBIE, such as copy number variations (CNVs) and tumor mutational burden (TMB), were significantly associated with tumor progression. In the experimental validation phase, we utilized small interfering RNA (siRNA) technology to silence NFKBIE expression in GBM cell lines, including U87 and T98G. Functional assays were then performed to assess the impact of NFKBIE knockdown. Cell proliferation assays, including CCK-8 and clonogenic assays, demonstrated that silencing NFKBIE significantly inhibited the proliferation of GBM cells. Migration and invasion assays, including wound healing and Transwell assays, further confirmed that NFKBIE knockdown markedly suppressed the migratory and invasive abilities of GBM cells. Additionally, apoptosis assays, such as TUNEL staining, revealed that NFKBIE silencing significantly promoted apoptosis in GBM cells. Western blot analysis confirmed the changes in the expression of key markers associated with proliferation, stemness, migration, invasion, and apoptosis. Furthermore, in a mouse xenograft model, NFKBIE knockdown significantly slowed tumor growth. Histological analysis of the excised tumors confirmed that reduced NFKBIE expression was closely associated with the inhibition of tumor growth. Notably, NFKBIE silencing also led to the downregulation of components of the Hedgehog signaling pathway, suggesting that NFKBIE may regulate tumor progression through modulation of this critical pathway. In conclusion, high NFKBIE expression is strongly associated with GBM progression and poor prognosis, and targeting its expression may offer a promising therapeutic strategy for GBM treatment.

Objective Carotid artery stenosis (CAS) is a significant contributor to cerebral ischemic events (CIEs). This study investigated the expression pattern and clinical significance of lncRNA NEXN-AS1 in CAS and CIEs. Methods 132 patients with CAS and 98 controls were enrolled. RT-qPCR was employed to quantify serum levels of NEXN-AS1 and miR-92a-1-5p. The diagnostic utility of NEXN-AS1 for CAS was assessed using ROC curves. Logistic regression pinpointed potential risk factors for severe CAS. Patients were followed for 2 years, and Kaplan-Meier and Cox methods evaluated the prognostic role of NEXN-AS1 and risk factors for CIEs in CAS cases. RIP and DLR assays were conducted to confirm the association between NEXN-AS1 and miR-92a-1-5p. Results Serum NEXN-AS1 was less expressed in CAS patients than in controls, which could effectively distinguish between the two groups with high sensitivity and specificity. CAS patients with severe stenosis had lower serum NEXN-AS1 levels than those with moderate stenosis. Patients with low NEXN-AS1 expression were more prone to developing CIEs compared to those with high expression (log-rank P = .0051). Cox regression analysis identified NEXN-AS1 as an independent risk factor for the development of CIEs. Molecularly, the target of NEXN-AS1 is miR-92a-1-5p. Conclusion Patients with low NEXN-AS1 expression could serve as diagnostic indicators for CAS and may predict the occurrence of CIEs. This study may offer new insights into the management of CAS and CIEs.

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Despite advances in acute care and neurological intensive care units, predicting long-term outcomes for patients with TBI remains challenging. Aquaporin-4 (AQP4) has emerged as a potential biomarker for assessing TBI severity and prognosis. Our goal is to evaluate AQP4 as a novel agent in the accurate diagnosis and prognosis of patients with TBI. This study included patients with TBI classified into mild (n = 80), moderate (n = 139), and severe (n = 96) groups based on Glasgow Coma Scale (GCS) scores. Cerebrospinal fluid (CSF) samples were collected at 1-, 7-, 14-, and 28-days postadmission, and AQP4 concentrations were measured using ELISA. The prognosis was evaluated using the Glasgow Outcome Scale (GOS) at 3 mo postinjury. The relationship between AQP4 levels and TBI severity, and their predictive value for patient outcomes, was analyzed. AQP4 levels in CSF peaked at 14 days postadmission and significantly decreased by 28 days in patients with both moderate and severe TBI. Higher AQP4 levels were consistently associated with worse prognosis at all measured time points. receiver operating characteristic (ROC) analysis revealed that AQP4 levels had predictive values at 1-, 7-, 14-, and 28-days postadmission, and the highest was shown at 14 days postadmission, with an area under the curve (AUC) of 0.79, sensitivity of 67.82%, and specificity of 83.78%. AQP4 in CSF is a promising biomarker for assessing TBI severity and predicting prognosis. Monitoring AQP4 levels could be an effective way to enhance prognostic accuracy, guide therapeutic interventions, and improve clinical decision-making in TBI management.NEW & NOTEWORTHY Our study is the first to comprehensively track dynamic changes in cerebrospinal fluid (CSF) aquaporin-4 (AQP4) levels in patients with moderate to severe traumatic brain injury. We show that AQP4 peaks at 14 days, correlates with injury severity, and consistently predicts 3-mo outcomes, with the strongest prognostic accuracy at day 14. These findings identify CSF AQP4 as a promising biomarker for assessing severity and prognosis, offering potential to improve early prediction and guide clinical decision-making in TBI management.

The clearance function is essential for maintaining brain tissue homeostasis, and the glymphatic system is the main pathway for removing brain interstitial solutes. Aquaporin-4 (AQP4) is the most abundantly expressed aquaporin in the central nervous system (CNS) and is an integral component of the glymphatic system. In recent years, many studies have shown that AQP4 affects the morbidity and recovery process of CNS disorders through the glymphatic system, and AQP4 shows notable variability in CNS disorders and is part of the pathogenesis of these diseases. Therefore, there has been considerable interest in AQP4 as a potential and promising target for regulating and improving neurological impairment. This review aims to summarize the pathophysiological role that AQP4 plays in several CNS disorders by affecting the clearance function of the glymphatic system. The findings can contribute to a better understanding of the self-regulatory functions in CNS disorders that AQP4 were involved in and provide new therapeutic alternatives for incurable debilitating neurodegenerative disorders of CNS in the future.

Background: Aquaporin 4 (AQP4), usually expressed at astrocytes end-feet, is a main component of the lymph-lymphatic system and promotes paravascular cerebrospinal fluid-interstitial fluid exchange. Moreover, angiotensin II type 1 (AT(1)) receptor affects amyloid beta (A beta) levels. This study aimed to detect the effect of AT, receptor deficiency on the blood-brain barrier (BBB) of traumatic brain injury (TBI) mice and the effect on A beta level and glial lymphatic circulation. Methods: TBI model was built using AT(1) receptor knockout mice (AT(1)-KO) and C57BL/6 mice (wild type, WT). BBB integrity was detected by Evans blue extravasation. The expression of the astrocytic water channel AQP4 and astrocyte activation were evaluated with immunofluorescence. The expressions of amyloid precursor protein (APP), junction protein zonula occludens protein-1 (ZO-1) and occludin in mice brain were detected by Western blot (WB). A beta levels were assayed by enzyme-linked immunosorbent assay (ELISA). Results: AT(1) receptor deficiency defended BBB integrity and rescued occludin and ZO-1 decrease in mice brain induced by TBI. AT(1)-KO mice had less increase of APP expression and A beta 1-42, A beta 1-40 levels compared to WT mice under TBI. Moreover, AT(1) receptor deficiency was found to significantly inhibit AQP4 depolarization after TBI. Conclusion: T-1 receptor deficiency attenuated TBI-induced impairments of BBB by rescuing tight junction proteins and inhibited AQP4 polarization, thus improving the function of glymphatic system to enhance interstitial A beta clearance in TBI mice brain.

右位主动脉弓是一种较为罕见的变异，通常合并弓上血管异常。河北医科大学第二医院神经外科2020年12月收治1例右位主动脉弓合并左侧椎动脉V2段狭窄、右侧颈内动脉颅外段重度狭窄的患者，采用左侧椎动脉V2段支架置入术、右侧颈内动脉内膜切除术治疗，患者症状明显改善，无相关并发症发生。

ObjectiveThe abnormal expression of matrix metalloproteinase 9 (MMP9) and Aquaporin 4 (AQP4) closely associates with the traumatic brain injury (TBI) development.MethodsHere, we investigated the relationship between miR-211-5p and MMP9/AQP4 axis in TBI patients and astrocyte cells. Demographics, clinical features, and cerebrospinal fluid (CSF) samples were collected from traumatic brain injury (TBI) patients (n = 96) and controls (n = 30) for pathological and gene expression analyses. Luciferase activity assay and gene expression analyses were performed to dissect the regulatory mechanism of miR-211-5p on MMP9/AQP4 in human astrocyte cells.ResultsmiR-211-5p mRNA was significantly decreased in the CSF of TBI patients, which positively correlated with the expression of both MMP9 and AQP4. miR-211-5p could target MMP9 directly in SVG P12 cells. Overexpression of miR-211-5p decreased the expression of MMP9, on the contrary, knockdown miR-211-5p through inhibitors increased the expression of both MMP9 and AQP4.ConclusionmiR-211-5p inhibits the MMP9/AQP4 axis in human astrocyte cells, which represents a promising approach for the TBI treatment.

Stent retriever thrombectomy (SRT) is one of the most effective methods for the recanalization of acute basilar artery occlusion (ABAO). The proatlantal intersegmental artery (PIA) is a rare carotid-vertebrobasilar anastomosis. Recognition of this rare form of anastomosis is particularly important for the rapid establishment of positive blood flow in patients with ABAO. In this case, the patient had a rare, left type 1 PIA. The right vertebral artery (VA) was tenuous and did not enter the cranium. We performed a thrombectomy of the ABAO by inserting a catheter via the type 1 PIA. The complete recanalization of basilar artery (BA) flow was achieved following two stent retractions; however, the patient eventually died of brain stem hemorrhage.

BACKGROUND:Traumatic brain injury (TBI) is a common clinical condition caused by external force. Aquaporin-4 (AQP4) in astrocytes participates in the generation of cell swelling in TBI. METHODS:This research explored the effect of AQP4 gene silencing in a TBI rat model. A hydraulic craniocerebral trauma instrument was employed for establishing the TBI rat model. AQP4 expression in the brain was inhibited by the injection of AQP4 shRNA-lentiviral vector. The expression of relative genes was evaluated by Western blot and qRT-PCR. Neuronal apoptosis was analyzed by TUNEL assay. RESULTS:AQP4 shRNA treatment inhibited AQP4 expression in the brain of rats with TBI. AQP4 shRNA alleviated TBI-induced brain edema and neurological deficit in rats. Neuronal apoptosis and astrocyte activation in TBI rats were reduced by AQP4 silencing. CONCLUSION:This research demonstrated that AQP4 shRNA-induced silencing of AQP4 in the TBI rat model reduced the expression of AQP4 and GFAP, alleviated brain edema, neurological deficit, neuronal apoptosis and inhibited astrocyte activation.

目的 探讨去骨瓣减压术后3w之内实施超早期颅骨修补术的安全性与可行性.方法 分析河北医科大学第二医院东院区神经外科2017.01-2021.06期间收治的159例颅骨修补患者临床资料,平均随访时间(27.21±14.44)月,其中超早期修补组(≤3w)23例,非超早期修补组136例(＞3w),比较两组在颅骨修补手术时间、术中出血量、手术相关并发症(术后伤口愈合、皮下积液、癫痫、感染、颅内血肿)之间的差别.结果 超早期组颅骨修补时间平均(112.39±22.71)min、明显短于非超早期组(146.19±20.02)min,两组之间比较差异有统计学意义(P=0.000).术中出血量超早期组平均(70.00±33.98)ml,非超早期组(87.39±88.87)ml,两组之间比较差异无统计学意义(P=0.519).超早期组手术相关并发症总发生率为13.04％(3/23),非超早期组为11.76％(16/136),两组之间比较差异无统计学意义(P=0.056).结论 术后3w内实施的超早期颅骨修补术所需的手术时间短、未增加术中出血量及手术相关并发症发生率,具有较高的安全性和可行性.

目的 研究将患者CT或MRI的DCM文件数据通过开发的软件处理,为大脑镰旁病变提供头皮投影定位的数据,准确定位手术切口.方法 该软件系统基于云平台部署,在浏览器内使用,对上传的患者头颅CT或MRI检查数据进行3D建模.创建水平位、矢状位和冠状位等3个视图加上3D视图,通过坐标转换,计算出眉间到大脑镰旁靶点的曲线长度,确认头皮表面的病变投影位置.结果 大脑镰旁病变手术患者均能成功准确定位,解决了因粗略定位不准而导致的不必要损伤.结论 通过软件计算处理患者CT或MRI检查的DCM文件数据,为大脑镰旁病变提供可靠定位数据,是一种简易而准确的大脑镰附近病变手术的头皮定位方法.

目的探讨细胞纤维连接蛋白（cFN）、白蛋白（Alb）/糖化血红蛋白（HbA1c）、干扰素-γ（IFN-γ）在创伤性脑出血患者行标准大骨瓣减压术（SLTC）围手术期的动态变化，及其与神经功能的关联性和在预测预后中的效能。 方法选取2017年5月—2020年2月该院行SLTC的创伤性脑出血患者219例，根据术后30 d预后情况，分为预后良好组（107例）和预后不良组（112例）。比较两组术前、术后第1、2和3天cFN、Alb/HbA1c、IFN-γ、美国国立卫生研究院卒中量表（NIHSS）、格拉斯哥昏迷量表（GCS）评分，并检验cFN、Alb/HbA1c、IFN-γ在预后预测中的价值。 结果预后良好组术后第1、2和3天cFN、IFN-γ低于预后不良组，Alb/HbA1c高于预后不良组（P 术后第3天>术后第1天，术后第7天各指标中预测预后的AUC，cFN最大（0.857），其次是Alb/HbA1c（0.825）、IFN-γ（0.824）（P 结论创伤性脑出血SLTC术患者术后早期cFN、IFN-γ呈升高趋势，Alb/HbA1c呈降低趋势，术后各时间点cFN、Alb/HbA1c、IFN-γ均与患者神经功能缺损、意识状态有关，检测术后第7天各指标水平能为临床预测预后提供重要的参考信息。

Pyroptosis has been reported to contribute to the traumatic brain injury (TBI) process. Ac-FLTD-CMK is a newly synthesized pyroptosis inhibitor. However, whether Ac-FLTD-CMK inhibits pyroptosis and plays a neuroprotective role after TBI is unknown. The present study aimed to determine the effects of Ac-FLTD-CMK on TBI in a mouse model. Male C57BL/6 mice were randomly divided into sham, TBI + vehicle, and TBI + Ac-FLTD-CMK groups. TBI was induced using a weight-drop apparatus. Intraventricular injection of Ac-FLTD-CMK was performed 30 min after TBI. Caspase-1, caspase-11, gasdermin-D (GSDMD), and caspase-3 expression in the peri-contusional cortex were assessed by western blotting. Interleukin-1β (IL-1β) and interleukin-18 (IL-18) expression in the peri-contusional cortex were measured using ELISA. Behavioral experiments, brain water content, Evans blue extravasation, lactate dehydrogenase (LDH) release, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining were also performed. The results showed that Ac-FLTD-CMK administration significantly downregulated caspase-1 p20, caspase-11 p20, GSDMD N-terminal, IL-1β, and IL-18 expression; reduced LDH release; alleviated neuronal death; attenuated brain edema and blood-brain barrier damage; and improved neurobehavioral function. These findings indicate that Ac-FLTD-CMK treatment suppresses pyroptosis and protects mice against TBI.

Background: Traumatic brain injury (TBI) has been a crucial health problem, with more than 50 million patients worldwide each year. Glymphatic system is a fluid exchange system that relies on the polarized water channel aquaporin-4 (AQP4) at the astrocytes, accounting for the clearance of abnormal proteins and metabolites from brain tissues. However, the dysfunction of glymphatic system and alteration of AQP4 polarization during the progression of TBI remain unclear. Methods: AQP4 −/− and Wild Type (WT) mice were used to establish the TBI mouse model respectively. Morris water maze (MWM) was used to establish the cognitive functions of AQP4 −/− and WT mice post TBI. Western-blot and qRT-PCR assays were performed to demonstrate protective effects of AQP4 deficiency to blood-brain barrier (BBB) integrity and amyloid-β clearance. The inflammation of cerebral tissues post TBI was estimated by ELISA assay. Results: AQP4 deficiency alleviated the brain edema and neurological deficit in TBI mice. AQP4-knockout led to improved cognitive outcomes in mice post TBI. The BBB integrity and cerebral amyloid-β clearance were protected by AQP4 deficiency in TBI mice. AQP4 deficiency ameliorated the TBI-induced inflammation. Conclusion: AQP4 deficiency improved longer-term neurological outcomes in a mouse model of TBI.